520 research outputs found
Bloom-Gilman duality of the nucleon structure function and the elastic peak contribution
The occurrence of the Bloom-Gilman duality in the nucleon structure function
is investigated by analyzing the Q**2-behavior of low-order moments, both
including and excluding the contribution arising from the nucleon elastic peak.
The Natchmann definition of the moments has been adopted in order to cancel out
target-mass effects. It is shown that the onset of the Bloom-Gilman duality
occurs around Q**2 ~ 2 (GeV/c)**2 if only the inelastic part of the nucleon
structure function is considered, whereas the inclusion of the nucleon elastic
peak contribution leads to remarkable violations of the Bloom-Gilman duality.Comment: in Proc. of the XVI European Conference on Few-body Problems in
Physics, Autrans (France), July 199
On Justification, Idealization, and Discursive Purchase
Conceptions of acceptability-based moral or political justification take it that authoritative acceptability, widely conceived, constitutes, or contributes to, validity, or justification. There is no agreement as to what bar for authoritativeness such justification may employ. The paper engages the issue in relation to (i) the level of idealization that a bar for authoritativeness, ψ, imparts to a standard of acceptability-based justification, S, and (ii) the degree of discursive purchase of the discursive standing that S accords to people when it builds ψ. I argue that (i) and (ii) are interdependent: high idealization values entail low discursive purchase, while high degrees of purchase require low idealization values. I then distinguish between alethic conceptions of justification that prioritize ends that commit to high idealization values, and recognitive conceptions that favor high discursive purchase. On this basis, I argue for a moderately recognitivist constraint on idealization. To render the recognitive discursive minimum available to relevant people at the site of justification, S should set ψ low enough so that it is a genuine option for actual people to reject relevant views in ways that S recognizes as authoritative. (The Appendix applies this to a Forst-type view of reciprocity of reasons to draw out some limitations of this view.) [Draft available from author on request.
CERN West Area neutrino facility beam line alignment
This papers describes the alignment of the West Area Neutrino Beam Line at CERN to the two neutrino experiments CHORUS and NOMAD. The T9 neutrino (n) target position and the position of the magnetic horn were optimised using the secondary muon intensity profiles from the muon pits in the shielding. In the experiments the improved geometry provides a better centred beam (< 5 cm) and a measured increase in the n flux of 8%
In non-transformed cells Bak activates upon loss of anti-apoptotic Bcl-X-L and Mcl-1 but in the absence of active BH3-only proteins
Mitochondrial apoptosis is controlled by proteins of the B-cell lymphoma 2 (Bcl-2) family. Pro-apoptotic members of this family, known as BH3-only proteins, initiate activation of the effectors Bcl-2-associated X protein (Bax) and Bcl-2 homologous antagonist/killer (Bak),which is counteracted by anti-apoptotic family members. How the interactions of Bcl-2 proteins regulate cell death is still not entirely clear. Here, we show that in the absence of extrinsic apoptotic stimuli Bak activates without detectable contribution from BH3-only proteins, and cell survival depends on anti-apoptotic Bcl-2 molecules. All anti-apoptotic Bcl-2 proteins were targeted via RNA interference alone or in combinations of two in primary human fibroblasts. Simultaneous targeting of B-cell lymphoma-extra large and myeloid cell leukemia sequence 1 led to apoptosis in several cell types. Apoptosis depended on Bak whereas Bax was dispensable. Activator BH3-only proteins were not required for apoptosis induction as apoptosis was unaltered in the absence of all BH3-only proteins known to activate Bax or Bak directly, Bcl-2-interacting mediator of cell death, BH3-interacting domain death agonist and p53-upregulated modulator of apoptosis. These findings argue for auto-activation of Bak in the absence of anti-apoptotic Bcl-2 proteins and provide evidence of profound differences in the activation of Bax and Bak
Vector Meson Photoproduction with an Effective Lagrangian in the Quark Model
A quark model approach to the photoproduction of vector mesons off nucleons
is proposed. Its starting point is an effective Lagrangian of the interaction
between the vector meson and the quarks inside the baryon, which generates the
non-diffractive s- and u- channel resonance contributions. Additional t-channel
and exchanges are included for the and
production respectively to account for the large diffractive behavior in the
small region as suggested by Friman and Soyeur. The numerical results are
presented for the and productions in four isospin channels with
the same set of parameters, and they are in good agreement with the available
data not only in and productions but also in the charged
productions where the additional t-channel exchange does not
contribute so that it provides an important test to this approach. The
investigation is also extended to the photoproduction, and the initial
results show that the non-diffractive behavior of the productions in the
large region can be described by the s- and u- channel contributions with
significantly smaller coupling constants, which is consistent with the findings
in the similar studies in the QHD framework. The numerical investigation has
also shown that polarization observables are essential for identifying
so-called "missing resonances".Comment: 36 pages, 10 PS figures, extended version of nucl-th/9711061 and
nucl-th/9803021, submitted to PR
MAJOR 1.5 - A Monte Carlo Generator for Heavy Majorana Neutrinos in Collisions
The Monte Carlo generator {\sc Major} 1.5 simulates the production and decay
of heavy Majorana neutrinos via lepton mixing or exchange of `light'
right-handed -bosons in deep inelastic scattering, i.e. or . Physics and
programming aspects are described in this manual.Comment: 13 pages LaTeX, 2 PostScript figure
In non-transformed cells Bak activates upon loss of anti-apoptotic Bcl-X-L and Mcl-1 but in the absence of active BH3-only proteins
Mitochondrial apoptosis is controlled by proteins of the B-cell lymphoma 2 (Bcl-2) family. Pro-apoptotic members of this family, known as BH3-only proteins, initiate activation of the effectors Bcl-2-associated X protein (Bax) and Bcl-2 homologous antagonist/killer (Bak),which is counteracted by anti-apoptotic family members. How the interactions of Bcl-2 proteins regulate cell death is still not entirely clear. Here, we show that in the absence of extrinsic apoptotic stimuli Bak activates without detectable contribution from BH3-only proteins, and cell survival depends on anti-apoptotic Bcl-2 molecules. All anti-apoptotic Bcl-2 proteins were targeted via RNA interference alone or in combinations of two in primary human fibroblasts. Simultaneous targeting of B-cell lymphoma-extra large and myeloid cell leukemia sequence 1 led to apoptosis in several cell types. Apoptosis depended on Bak whereas Bax was dispensable. Activator BH3-only proteins were not required for apoptosis induction as apoptosis was unaltered in the absence of all BH3-only proteins known to activate Bax or Bak directly, Bcl-2-interacting mediator of cell death, BH3-interacting domain death agonist and p53-upregulated modulator of apoptosis. These findings argue for auto-activation of Bak in the absence of anti-apoptotic Bcl-2 proteins and provide evidence of profound differences in the activation of Bax and Bak
Verifiable Model of Neutrino Masses from Large Extra Dimensions
We propose a new scenario of neutrino masses with a Higgs triplet
in a theory of large extra dimensions. Lepton number
violation in a distant brane acts as the source of a very small trilinear
coupling of to the standard Higgs doublet in our brane. Small realistic
Majorana neutrino masses are \underline{naturally} obtained with the
fundamental scale TeV, foretelling the possible
discovery of (m_\xi\lsim M_*) at future colliders. Decays of
into same-sign dileptons are fixed by the neutrino mass matrix. Observation of
conversion in nuclei is predicted.Comment: A comment on Tevatron reach and two references added. Discussion and
conclusions unchange
Parton model versus color dipole formulation of the Drell-Yan process
In the kinematical region where the center of mass energy is much larger than
all other scales, the Drell-Yan process can be formulated in the target rest
frame in terms of the same color dipole cross section as low Bjorken-x deep
inelastic scattering. Since the mechanisms for heavy dilepton production appear
very different in the dipole approach and in the conventional parton model, one
may wonder whether these two formulations really represent the same physics. We
perform a comparison of numerical calculations in the color dipole approach
with calculations in the next-to-leading order parton model. For proton-proton
scattering, the results are very similar at low x_2 from fixed target to RHIC
energies, confirming the close connection between these two very different
approaches. We also compare the transverse momentum distributions of Drell-Yan
dileptons predicted in both formulations. The range of applicability of the
dipole formulation and the impact of future Drell-Yan data from RHIC for
determining the color dipole cross section are discussed. A detailed derivation
of the dipole formulation of the Drell-Yan process is also included.Comment: 20 pages, 5 figure
Hard diffraction in hadron--hadron interactions and in photoproduction
Hard single diffractive processes are studied within the framework of the
triple--Pomeron approximation. Using a Pomeron structure function motivated by
Regge--theory we obtain parton distribution functions which do not obey
momentum sum rule. Based on Regge-- factorization cross sections for hard
diffraction are calculated. Furthermore, the model is applied to hard
diffractive particle production in photoproduction and in
interactions.Comment: 13 pages, Latex, 13 uuencoded figure
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